Biologically active vitamin D.sub.3 and vitamin D.sub.2 materials, due to their action in increasing serum calcium have been utilized in the treatment of various calcium metabolic disorders. Among these disorders include chronic renal disease, Vitamin D resistant rickets, glucocorticord-induced decrease in calcium absorption, osteoporosis, senile decrease in calcium absorption, hypoparathyroidism, turkey weak leg diseases, milk fever diseases, and the like. In the past, biologically active Vitamin D.sub.3 and Vitamin D.sub.2 materials have been administered to patients orally or intravenously.
A danger in administering biologically active vitamin D.sub.3 and vitamin D.sub.2 materials orally or intravenously to patients is that the therapeutic to toxic ratio (therapeutic index) of this drug is low and an excess of the drug in the blood stream, especially after administration, can cause episodes of hypercalcemia and hypercalcuria. While hypercalcemia and hypercalcuria can be corrected to a large degree by decreasing the dose of the drug, there is always the danger of hypercalcemia and hypercalcuria repeatedly occuring each time a patient receives a given oral or intravenous dose. This is believed due to the fact that immediately after administration of these drugs, the drug is transported in high concentrations across the small intestine which is one of the principal sites of activity for these drugs. Thus, especially after oral administration, the small intestine is initially exposed to very high concentrations of these metabolites which in turn could induce a very rapid uncontrolled rise in intestinal calcium transport which is reflected in high serum calcium levels in the blood.
Therefore, it has been desired to provide a means for administering biologically active vitamin D.sub.3 or vitamin D.sub.2 materials to avoid the uncontrolled increase in serum calcium levels which could occur immediately after administration of the biologically active vitamin D.sub.3 and vitamin D.sub.2 materials.